Cappariloside A
Cappariloside A is a larvicide that exhibits larvicidal activity against Aedes aegypti larvae and reduces larval glutathione-S-transferase activity. Cappariloside A also possesses antiviral activity, decreases the level of phosphorylated STAT1 in cells, inhibits the replication of influenza viruses H1N1, H3N2, PIV3 and ADV, and downregulates the expression of IL-6, IP-10, MIG, RANTES/CCL-5, IFN-β and IL-29. Cappariloside A suppresses the inflammatory response induced by mouse lung-adapted influenza virus strains. Cappariloside A can be used in studies related to larvicidal applications and influenza virus infection.
For research use only. We do not sell to patients.
- CAS No.: 229483-41-4
- Formula: C16H18N2O6
- Molecular Weight:334.32
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
Cappariloside A (Compound 1) (24-48 h) exhibits larvicidal activity against 3rd-instar *Aedes aegypti* larvae, with an LC50 value of 71.14 ppm[1].
Cappariloside A (71.14 ppm; 24 h) reduces the activity of glutathione-S-transferase in surviving 3rd-instar *Aedes aegypti* larvae[1].
Cappariloside A (0-400 μg/mL; 72 h) inhibits the replication of influenza A virus strain A/PR/8/34 (H1N1) in MDCK cells, with an IC50 value of 115.25 μg/mL[2].
Cappariloside A (48 h) exhibits potent antiviral activity against human influenza virus subtypes A/PR/8/34 (H1N1), A/GZ/GIRD07/09 (H1N1 pdm2009) and A/HK/8/68 (H3N2) in MDCK cells, with IC50 values of 288.03, 362.18 and 375.73 μg/mL, and SI values of 4.36, 3.37 and 3.34, respectively[2].
Cappariloside A exhibits antiviral activity against PIV3 in LLC-MK2 cells (IC50 = 757.86 μg/mL, SI = 1.32), and against ADV3 in A549 cells (IC50 = 382.23 μg/mL, SI = 3.32)[2].
Cappariloside A (0-4 mg/mL; 6-72 h) inhibits the progeny replication of influenza A virus strain A/PR/8/34 (H1N1) in 16HBE cells, and suppresses virus-induced expression of IL-6, IP-10, MCP-1 and RANTES/CCL-5 at doses as low as 0.25 mg/mL[2].
Cappariloside A (0.25-2 mg/mL; 24, 48 h) inhibits the progeny replication of influenza A virus A/PR/8/34 (H1N1) in RAW264.7 cells, and suppresses the virus-induced expression of IP-10 and RANTES/CCL-5 at concentrations of 1 mg/mL and 0.5 mg/mL[2].
Cappariloside A (0-1 mg/mL; 24 h) inhibits the expression of IP-10 and RANTES/CCL-5 in 16HBE cells induced by avian influenza virus H9N2, but does not suppress viral replication[2].
Cappariloside A (0-2 mg/mL; 24 h) inhibits LPS (HY-D1056)-induced expression of IP-10, IL-6 and RANTES/CCL-5 in RAW264.7 cells without affecting TNF-α levels[2].
Cappariloside A (0-2 mg/mL; 6, 24, 48, 72 h) regulates the host IFN signaling pathway in 16HBE cells by inhibiting virus-induced STAT1 phosphorylation, reducing the expression of IFN-β and IL-29, and suppressing IFN-β-induced expression of IP-10 and RANTES/CCL-5[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Human bronchial epithelial (16HBE) cells infected with avian influenza virus A/Chicken/Guangdong/1996 (H9N2)
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Concentration:1, 0.5, 0.25 mg/mL
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Incubation Time:24 h
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Result:Significantly reduced H9N2-induced protein levels of IP-10 and RANTES/CCL-5 in a dose-dependent manner, despite no inhibition of H9N2 replication.
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Cell Line:Murine macrophage (RAW264.7) cells stimulated with lipopolysaccharide (LPS)
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Concentration:2, 1 mg/mL
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Incubation Time:24 h
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Result:Significantly reduced LPS-induced protein levels of IP-10, IL-6, and RANTES/CCL-5 in a dose-dependent manner, with no effect on TNF-α levels.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (female, 6-8 weeks old)[2]
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Dosage:75-300 mg/kg/day
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Administration:p.o.; twice daily; 5 days
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Result:Inhibited influenza-induced weight loss at day 3, 5, and 7 post-infection at 300 mg/kg·day; inhibited influenza-induced weight loss at day 3 post-infection at 150 and 75 mg/kg·day.
Reduced pulmonary index by 50% at day 5 post-infection at 300 mg/kg·day; reduced pulmonary index by 30% at day 5 post-infection at 150 mg/kg·day; reduced pulmonary index by 20% at day 5 post-infection at 75 mg/kg·day.
Inhibited total protein concentration increase in bronchoalveolar lavage fluid (BALF) at day 3, 5, and 7 post-infection at 300 mg/kg·day; inhibited total protein concentration increase in BALF at day 3, 5, and 7 post-infection at 150 mg/kg·day; inhibited total protein concentration increase in BALF at day 3 and 5 post-infection at 75 mg/kg·day.
Reduced inflammatory cell infiltration, inflammatory area, and pathology score in lung tissue at 300 mg/kg·day.
Decreased total white cell counts in BALF at day 5 post-infection at 300, 150, and 75 mg/kg·day.
Inhibited influenza-induced IL-6 and IP-10 levels in BALF at day 3, 5, and 7 post-infection at 300 mg/kg·day; inhibited influenza-induced IL-6 and IP-10 levels in BALF at day 3 and 5 post-infection at 150 and 75 mg/kg·day.
Chemical Information
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CAS No. 229483-41-4
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Molecular Weight 334.32
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Formula C16H18N2O6
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SMILES
N#CCC1=CNC2=CC=CC(O[C@@H]3O[C@@H]([C@H]([C@@H]([C@H]3O)O)O)CO)=C21
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Cappariloside A Related Classifications
HY-N17963 Related Classifications
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